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Coronary Perfusion Pressure (coronary + perfusion_pressure)

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Medical Sciences	100%

Selected Abstracts

Endothelin-1-mediated coronary vasoconstriction deteriorates myocardial depression in hearts isolated from lipopolysaccharide,treated rats: Interaction with nitric oxide

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2004
Jie Tu
Summary 1.,The aim of the present study was to evaluate the contribution of disturbance of coronary perfusion to myocardial depression in hearts isolated from lipopolysaccharide (LPS)-treated rats and to investigate the involvement of endothelin (ET)-1 and nitric oxide (NO). 2.,Rats were treated with LPS (10 mg/kg, i.p.) and, 4 h later, plasma ET-1 concentrations were measured by radioimmunoassay and hearts were excised for perfusion at a constant perfusion flow. The selective ETA receptor antagonist BQ-123, in the absence or presence of aminoguanidine, a specific inhibitor of inducible NO synthase, was given 15 min before LPS challenge. Coronary perfusion pressure (CPP) and measures of myocardial contractile function were recorded. 3.,In hearts isolated from LPS-treated rats, there was a marked increase in CPP that was abolished by pretreatment with BQ-123. In parallel, an increase in plasma ET-1 concentrations was seen in these rats. Lipopolysaccharide also induced decreases in left ventricular developed pressure (LVDP), the product of LVDP and heart rate and maximal rate of rise/fall of left ventricular pressure (+/, dP/dtmax). Single treatment with BQ-123 or aminoguanidine attenuated LPS-induced myocardial depression. However, when these two drugs were given simultaneously, myocardial depression elicited by LPS was blocked significantly. 4.,Endothelin-1-mediated coronary vasoconstriction, together with NO, contributes to myocardial depression in hearts isolated from LPS-treated rats. [source]

Neurological outcome after experimental cardiopulmonary resuscitation: a result of delayed and potentially treatable neuronal injury?

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2002
X. L. Liu
Background: In experimental cardiopulmonary resuscitation (CPR) aortic balloon occlusion, vasopressin, and hypertonic saline dextran administration improve cerebral blood flow. Free radical scavenger ,-phenyl-N-tert-butyl-nitrone (PBN) and cyclosporine-A (CsA) alleviate neuronal damage after global ischemia. Combining these treatments, we investigated neurological outcome after experimental cardiac arrest. Methods: Thirty anesthetized piglets, randomly allocated into three groups, were subjected to 8 min of ventricular fibrillation followed by 5 min of closed-chest CPR. The combined treatment (CT) group received all the above-mentioned modalities; group B was treated with balloon occlusion and epinephrine; and group C had sham balloon occlusion with epinephrine. Indicators of oxidative stress (8-iso-PGF2,), inflammation (15-keto-dihydro-PGF2,), energy crisis (hypoxanthine and xanthine), and anoxia/hypoxia (lactate) were monitored in jugular bulb venous blood. Neurological outcome was evaluated 24 h after CPR. Results: Restoration of spontaneous circulation (ROSC) was more rapidly achieved and neurological outcome was significantly better in the CT group, although there was no difference in coronary perfusion pressure between groups. The jugular venous PCO2 and cerebral oxygen extraction ratio were lower in the CT group at 5,15 min after ROSC. Jugular venous 8-iso-PGF2, and hypoxanthine after ROSC were correlated to 24 h neurological outcome Conclusions: A combination of cerebral blood flow promoting measures and administration of ,-phenyl-N-tert-butyl-nitrone and cyclosporine-A improved 24 h neurological outcome after 8 min of experimental normothermic cardiac arrest, indicating an ongoing neuronal injury in the reperfusion phase. [source]

Carbon Monoxide Has Direct Toxicity on the Myocardium Distinct from Effects of Hypoxia in an Ex Vivo Rat Heart Model

ACADEMIC EMERGENCY MEDICINE, Issue 1 2008
Selim Suner MD
Abstract Objectives:, Carbon monoxide (CO) toxicity causes significant central nervous system and cardiac injury. Although the neurological damage caused by CO toxicity is extensively described, the mechanisms underlying myocardial insult are unclear. The authors used an externally perfused isolated rat heart model to examine the effects of a physiological saline solution (Krebs Henseleit HEPES, KHH) aerated with CO on cardiac function. Methods:, Fifteen rats were equally divided into three groups: the control group (KHH + 100% O2), the nitrogen control group (KHH + 70% O2, 30% N2), and the CO group (KHH + 70% oxygen, 30% CO). Left ventricular peak systolic pressure (LVPsP), end diastolic pressure (LVEdP), and coronary perfusion pressure were measured while the isolated heart was paced and perfused on a modified Langendorf apparatus. Results:, Left ventricular generated pressure (LVGP = LVPsP , LVEdP) decreased in the nitrogen control and CO groups compared to the control group. There was higher LVGP in the recovery phase between the nitrogen control group compared to the CO group. Both groups had increased lactic acid levels in the experimental phase. Conclusions:, Carbon monoxide with hypoxia and hypoxemic hypoxia both result in similar depression of cardiac function. Hearts poisoned with CO with hypoxia do not recover function to the extent that hearts rendered hypoxic with nitrogen do when perfused with 100% oxygen after the insult. This suggests that CO causes direct myocardial toxicity distinct from the effects of hypoxia. [source]

Coronary Blood Flow Produced by Muscle Contractions Induced by Intracardiac Electrical CPR during Ventricular Fibrillation

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2009
HAO WANG M.D.
It has been reported that transthoracic electrical cardiopulmonary resuscitation (ECPR) generates coronary perfusion pressures (CPP) similar to manual chest compressions (MCC). We hypothesized that intracardiac ECPR produces similar CPP. Methods: ECPR pulse train protocols were applied for 20 seconds in a porcine model following 10 seconds of ventricular fibrillation (VF), using a defibrillator housing electrode and a right ventricular coil (IC-ECPR). Each protocol consisted of 200-ms electrical pulse trains applied at a rate of 100 pulse trains/min. The protocols were grouped in skeletal-based versus cardiac-based stimulation measurements. CPP was recorded and compared to historical MCC values generated by a similar experimental design. CPP > 15 mm Hg at 30 seconds of VF following the application of an IC-ECPR protocol was defined as successful. Results: Mean CPP for all intracardiac ECPR pulse train protocols at 30 seconds of VF was 14.8 ± 3.8 mm Hg (n = 39). Mean CPP in seven successful skeletal-based IC-ECPR protocols was 19.4 ± 3.2 mm Hg, and mean CPP in 10 successful cardiac-based IC-ECPR protocols was 17.4 ± 2.1 mm Hg. Reported CPP for 15 MCC experiments at 30 seconds of VF was 22.9 ± 9.4 mm Hg (P = 0.35 compared to skeletal-based IC-ECPR, P = 0.08 compared to cardiac-based IC-ECPR). Conclusions: Intracardiac applied electrical CPR produced observable skeletal muscle contractions, measurable pressure pulses, and coronary perfusion pressures similar to MCC during a brief episode of untreated VF. [source]